![]() In a recent postmortem study of fatal falciparum malaria in adults, the median ratio of cerebral to peripheral blood parasitaemia was 40 (range 1.8–1500). 8 9 The peripheral blood parasite count is a relatively poor predictor of the size of this biomass. 7 It is the sequestered parasites that cause pathology in severe malaria, and prognosis is related to sequestered biomass. The sequestration of PRBCs in the relatively hypoxic venous beds allows optimal parasite growth and prevents the PRBCs from being destroyed by the spleen. 6 This process varies considerably between organs (the brain is particularly affected) and at a microvascular level varies between vessels. The sequestration of red cells containing mature forms of the parasite (trophozoites and meronts) in the microvasculature is thought to cause the major complications of falciparum malaria, particularly cerebral malaria. Ring stages are seen in the peripheral blood, but trophozoites and meronts are usually absent, as they are sequestered within the deep vascular beds. The merozoites released by the liver invade the erythrocyte, and during a period of 48 hours, pass through morphologically distinct stages, before the meronts (schizonts) rupture the erythrocyte. In humans, although the parasite undergoes development in the liver, it is the erythrocytic cycle that is responsible for disease. P falciparum is transmitted by female Anopheles mosquitoes. Severe malaria is a multisystem disease, and the outcome often depends on the degree of vital organ dysfunction. Metabolic acidosis, mainly a lactic acidosis, is common at all ages. In older children seizures and cerebral malaria predominate whereas in adults acute renal failure, acute pulmonary oedema, liver dysfunction, and cerebral malaria may all occur. 1 In the first 2 years of life severe anaemia is a common presenting feature of severe malaria. The manifestations of severe malaria differ depending on the age of the patient and previous exposure. Severe malaria occurs predominantly in patients with little or no background immunity-that is, children growing up in endemic areas, or travellers or migrants who come from areas without malaria, but are exposed to malaria later in life. There are four species of human malaria, but Plasmodium falciparumcauses nearly all the deaths and neurological complications. ![]() Malaria affects about 5% of the world's population at any time and causes somewhere between 0.5 and 2.5 million deaths each year. Malaria is the most important of the parasitic diseases of humans, and its neurological complication, cerebral malaria is arguably one of the most common non-traumatic encephalopathies in the world. ![]() Neurological sequelae are increasingly recognised, but further research on the pathogenesis of coma and neurological damage is required to develop other ancillary treatments. With appropriate antimalarial drugs, the prognosis of cerebral malaria often depends on the management of other complications-for example, renal failure and acidosis. Artemisinin derivatives have made an impact on treatment, but other drugs may be required. Antimalarial drugs, however, remain the only intervention that unequivocally affects outcome, although increasing resistance to the established antimalarial drugs is of grave concern. Recent studies have elucidated the molecular mechanisms of pathogenesis and raised possible interventions. The clinical presentation and pathophysiology differs between adults and children. The pathogenesis is heterogenous and the neurological complications are often part of a multisystem dysfunction. Cerebral malaria may be the most common non-traumatic encephalopathy in the world. ![]()
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